LINC00907 suppresses malignant progression in hepatocellular carcinoma by inhibiting miR-24-3p

Abstract Objective This study aimed to clarify the role of LINC00907 in hepatocellular carcinoma (HCC) and its underlying molecular mechanisms. Methods The research population comprised 117 participants diagnosed with HCC. The expressions of LINC00907 and miR-24-3p in both tissue specimens and cell lines, along with those of EMT markers and the MMP-2 and MMP-9, were measured using RT-qPCR. Cellular proliferation was measured with the CCK-8 assay, while apoptotic rates were determined by flow cytometry. The direct interactions between LINC00907, miR-24-3p, and PDGFRL were validated by dual luciferase reporter and RNA pull-down assays. HCC cells were transfected with constructs specifically modulating LINC00907 and miR-24-3p to investigate the impact of their expression on malignant phenotypic behaviors. Results LINC00907 expression was significantly downregulated in HCC, whereas miR-24-3p expression was upregulated. Low LINC00907 expression was linked to significantly worse overall survival, as determined by Kaplan-Meier analysis. The upregulation of LINC00907 led to the suppression of cell proliferation and EMT, while inducing apoptosis and reducing the levels of MMP-2 and MMP-9. LINC00907 was shown to directly target and negatively regulate miR-24-3p. Furthermore, rescue experiments demonstrated that upregulation of miR-24-3p counteracted the tumor-suppressive effects mediated by LINC00907 overexpression in HCC cells. Conclusion LINC00907 exerts tumor-suppressive effects by targeting and negatively regulating miR-24-3p, thereby influencing proliferation, apoptosis, and EMT in HCC cells.